Standard electrocardiography in pediatric practice

Health status

Right ventricular hypertrophy

(
RVH
) is a condition defined by abnormal enlargement of the heart muscle surrounding the right ventricle. The right ventricle is one of the four chambers of the heart. It is located at the bottom of the heart and receives blood from the right atrium and pumps blood to the lungs.

Because RVH is muscle enlargement, it occurs when the muscle requires more intense work. Therefore, the main causes of RVH are pathologies of systems associated with the right ventricle, such as the pulmonary artery, tricuspid valve, or airway.

RVH may be benign and have little impact on daily life, or may lead to conditions such as heart failure, with a poor prognosis.

Signs and symptoms[edit]

Symptoms[edit]

Although presentations vary, people with right ventricular hypertrophy may experience symptoms associated with pulmonary hypertension, heart failure, and/or reduced cardiac output. These include: [1] [2]

• Difficulty breathing during exercise
• Chest pain (angina) with exertion
• Fainting (fainting) on ​​exertion
• General fatigue/lethargy
• Dizziness
• Feeling of fullness in the upper abdomen
• Discomfort or pain in the right upper abdomen
• Decreased appetite
• Swelling (edema) of the legs, ankles, or feet
• Palpitations (palpitations)

People may rarely exhibit symptoms of Ortner syndrome, which include cough, hemoptysis, and hoarseness. [ citation needed

]

Signs[edit]

On physical examination, the most prominent findings are associated with the development of right-sided heart failure. These may include increased jugular venous pressure, ascites, left parasternal heave, and a tender, enlarged liver to palpation. [3] On examination, patients may be chronically ill, with cyanosis, cachexia and sometimes jaundice. [ citation needed

]

On auscultation, an increased second pulmonary sound (S2), a third heart sound called the “right ventricular gallop”, and a systolic murmur at the tricuspid valve, increased with inspiration, may be present. Sometimes a systolic murmur can be transmitted and heard through the liver. Less commonly, a diastolic murmur may also be heard as a result of pulmonary insufficiency. [3]

Reasons [edit]

RVH usually occurs due to chronic lung disease or structural heart defects. One of the most common causes of RVH is pulmonary hypertension (PH) [3], defined as an increase in blood pressure in the vessels that carry blood to the lungs. PH leads to increased pulmonary artery pressure. The right ventricle tries to compensate for this increased pressure by changing its shape and size. Hypertrophy of individual myocytes leads to an increase in the thickness of the wall of the right ventricle. [3] The incidence of PH worldwide is 4 per million people. [4] RVH occurs in approximately 30% of these cases. [ citation needed

]

The World Health Organization broadly classifies PH into five categories based on the underlying cause. The incidence of RVH varies between groups. Common causes of PH include chronic obstructive pulmonary disease (COPD), pulmonary embolism, and other restrictive lung diseases. RVH often occurs as a result of these disorders. RVH occurs in 76% of patients with advanced COPD and 50% of patients with restrictive lung disease. [3]

RVH also occurs as a result of structural defects of the heart. One common cause is tricuspid insufficiency. This is a condition in which the tricuspid valve does not close properly, causing blood to flow back. Other structural defects that lead to RVH include tetralogy of Fallot, ventricular septal defects, pulmonary valve stenosis, and atrial septal defects. [5] RVH is also associated with abdominal obesity, elevated fasting blood glucose, high systolic blood pressure, and partial shortening of the left ventricular medial wall. [ citation needed

]

Other risk factors for RVH include smoking, sleep apnea, and physical activity. They increase the risk of heart and lung disease and therefore RVH. [6]

What does the treatment consist of?

The initial stage of the treatment process is electrocardiographic diagnostics, which helps to identify the problem. An ultrasound may also be needed.

Due to the fact that hypertrophic changes in the ventricle are not an independent disease, but only a manifestation of some disorder, the maximum therapeutic effect can be achieved only by eliminating the underlying disease.

Drug treatment

In many ways, the treatment regimen depends on the stage of the pathological process. If the problem was identified at the compensated stage, then usually the disorder does not require special treatment. In this case, it is enough to follow certain recommendations to maintain heart function, namely:

• correct work and rest schedule;
• moderate physical exercise without overload;
• normalization of body weight;
• a balanced diet that includes a large amount of vitamins and unsaturated fats;
• giving up bad habits, in particular smoking and alcohol abuse.

Sometimes people with ventricular hypertrophy are given a disability group

In order to prevent further development of cardiac muscle overload, the following medications are prescribed:

• Atenolol or Metoprolol. These drugs restore heart rhythm and also reduce the oxygen demand of cells;
• Diltiazem or Verapamil. Prescribed to maintain normal blood pressure in blood vessels;
• Diroton or Enalapril. Effectively fight high blood pressure and heart failure;
• Losartan, Candesartan - reduce the mass of hypertrophied muscles.

Since the disorder is often accompanied by breathing problems, you will need to use drugs aimed at improving respiratory function:

• bronchodilators are drugs that improve the patency of the bronchi and increase their lumen;
• anti-inflammatory drugs normalize the functioning of the bronchi;
• drugs that reduce high pressure in the pulmonary artery.

The following can be said about the effectiveness of the treatment process:

• the size of the ventricle on the control study is much smaller;
• symptoms of heart failure disappear;
• there is a need to remove disability and restore working capacity;
• hypertensive crises, as well as attacks of angina pectoris and arrhythmia, pass;
• quality of life improves.

Drug therapy copes well with symptoms, but generally does not affect the etiological factor

Surgery

Surgical intervention is a last resort, which is resorted to only after the ineffectiveness of conservative methods or when severe heart defects are associated. The operation is usually performed at an early age. With the help of surgical intervention, a specialist acts on the root cause of the disorder.

Let's consider two main types of surgical intervention:

• aortic valve replacement. The operation is performed in two ways: either the chest is opened - this is a traditional technique, or the femoral artery is punctured - this is a minimally invasive intervention;
• prosthetics of not only the valve, but also the aortic part. Compared to the first type, this procedure is more traumatic and requires serious surgeon skills. In this case, either artificial prostheses or biological ones, made from pig tissue, are used.

Sometimes treatment is only possible after a heart transplant. This is a rather serious procedure that requires a large number of compatibility tests. In addition, even after the operation itself, the use of medications is required that will prevent rejection of the donor organ.

Allergy sufferers should use traditional recipes with caution

Traditional treatment

You should not reassure yourself by thinking that unconventional recipes will save you from the problem; miracles will not happen. It will not be possible to return the ventricles to their previous size and restore their previous function, but still folk recipes help lower blood pressure, strengthen the vascular wall and improve the contractility of the heart muscle.

It is best to buy medicinal plants in a pharmacy chain, where you are confident in the quality, correct collection and drying of the product. Let's look at three popular recipes:

• tincture of lily of the valley. The flowers of the plant should be placed in a dark glass container and filled with vodka. The product should infuse for two weeks. Once the tincture is filtered, it is ready for use. Take twenty drops three times a day;
• garlic tincture with the addition of honey and lemon helps stop atherosclerotic changes in blood vessels;
• St. John's wort decoction. For one hundred grams of dry St. John's wort, two liters of boiling water is used. After straining, you can add a small amount of honey. It is recommended to store in the refrigerator. People with serious liver disorders should not take this decoction.

So, despite the fact that ventricular hypertrophy is not a separate disease, its manifestation must be taken into account in the diagnosis of heart disease and subsequent treatment. The pathological process can lead to serious complications, including cardiac arrest. That is why you should regularly undergo a medical examination, and if you have any alarming symptoms from the heart, do not delay visiting a cardiologist.

Pathophysiology[edit]

Right ventricular hypertrophy can be either a physiological or pathophysiological process. It becomes pathophysiological (damaging) with excessive hypertrophy. The pathophysiological process mainly occurs through aberrant neuroendocrine hormone signaling; angiotensin II, endothelin-1 and catecholamines (such as norepinephrine). [ citation needed

]

Angiotensin-II and endothelin-1[edit]

Angiotensin-II and endothelin-1 are hormones that bind to the angiotensin (AT) and endothelin (ET) receptors. These are G protein-coupled receptors that act through intrinsic signaling pathways. Through several intermediates, these pathways directly or indirectly increase the production of reactive oxygen species (ROS), causing accumulation in myocardial cells. This may subsequently cause necrotic cell death, fibrosis, and mitochondrial dysfunction. [7]

This has been demonstrated in animal studies. Protein kinase C (PKC) is an intermediate molecule in the signaling pathway, and mice lacking PKC have shown resistance to heart failure compared to mice overexpressing PKC, which exhibit cardiac dysfunction. [8]

Targeting the renin-angiotensin system (RAAS) (using angiotensin-converting enzyme inhibitors and angiotensin receptor blockers) is a well-established clinical approach for reversing maladaptive cardiac hypertrophy, independent of blood pressure. [ citation needed

]

Catecholamines[edit]

Catecholamine levels increase due to increased activity of the sympathetic nervous system. Catecholamines can act on alpha-adrenergic receptors and beta-adrenergic receptors, which are G protein-coupled receptors. This binding initiates the same intracellular signaling pathways as angiotensin and endothelin. There is also activation of cAMP and an increase in intracellular Ca2+, which leads to contractile dysfunction and fibrosis. [7]

Other[edit]

Hormones are not the only cause of RVH. Hypertrophy can also be caused by mechanical forces, mTOR pathways, nitric oxide, and immune cells. Immune cells can cause hypertrophy by causing inflammation. [7]

Diagnosis[edit]

Hexaxial reference system

ECG shows right axis deviation

The two main diagnostic tests used to confirm right ventricular hypertrophy are electrocardiography and echocardiography. [ citation needed

]

Electrocardiography[edit]

The use of an electrocardiogram (ECG) to measure cardiac chamber hypertrophy is well established, but because left ventricular activity is dominant on the ECG, a large degree of RVH is often required for any detectable changes. However, ECG is used to diagnose RVH. A post-mortem study on 51 adult male patients concluded that anatomical RVH can be diagnosed using one or more of the following ECG criteria: [9]

• Axis deviation to the right is greater than (or equal to) 110° (see hex reference picture)
• The R wave is dominant over the S wave in V1 or V2
• The S wave is dominant over the R wave in V6

However, the American Heart Association recommended the use of additional diagnostic tests to diagnose RVH because no single criterion or set of criteria was considered sufficiently reliable. [10]

Echocardiography[edit]

Echocardiography can be used to directly visualize the wall thickness of the right ventricle. The preferred method is the transesophageal approach, which provides a view of 4 chambers. The normal thickness of the free wall of the right ventricle is from 2 to 5 millimeters, with a value above 5 mm being considered hypertrophic. [eleven]

Standard electrocardiography in pediatric practice

Electrocardiography (ECG) remains one of the most common methods for examining the cardiovascular system and continues to develop and improve. Based on the standard electrocardiogram, various modifications of the ECG have been proposed and are widely used: Holter monitoring, high-resolution ECG, tests with dosed physical activity, drug tests [2, 5].

Leads in electrocardiography

The concept of “electrocardiogram lead” means recording an ECG when electrodes are applied to certain areas of the body that have different potentials. In practical work, in most cases, registration of 12 leads is limited: 6 from the limbs (3 standard and 3 “unipolar reinforced”) and 6 thoracic leads - unipolar. The classic lead method proposed by Einthoven is the registration of standard limb leads, designated by Roman numerals I, II, III [6].

Enhanced limb leads were proposed by Goldberg in 1942. They record the potential difference between one of the limbs on which the active positive electrode of a given lead is installed (right arm, left arm or left leg), and the average potential of the other two limbs. These leads are designated as follows: aVR, aVL, aVF. The designations for augmented limb leads come from the first letters of English words: a - augmented (reinforced), V - voltage (potential), R - right (right), L - left (left), F - foot (leg).

Unipolar chest leads are designated by the Latin letter V (potential, voltage) with the addition of the position number of the active positive electrode, indicated in Arabic numerals:

lead V1 is an active electrode located in the fourth intercostal space along the right edge of the sternum;

V2 - in the fourth intercostal space along the left edge of the sternum;

V3 - between V2 and V4;

V4 - in the fifth intercostal space along the left midclavicular line;

V5 - in the fifth intercostal space along the anterior axillary line;

V6 - in the fifth intercostal space in the midaxillary line.

Using the chest leads, you can judge the condition (size) of the heart chambers. If the usual program for recording 12 generally accepted leads does not allow one to reliably diagnose a particular electrocardiographic pathology or requires clarification of some quantitative parameters, additional leads are used. These could be leads

V7 - V9, right chest leads - V3R-V6R [6].

Electrocardiogram recording technique

The ECG is recorded in a special room, remote from possible sources of electrical interference. The study is carried out after a 15-minute rest on an empty stomach or no earlier than 2 hours after a meal. The patient should be undressed to the waist, the lower legs should be freed from clothing. Electrode paste must be used to ensure good skin contact with the electrodes. Poor contact or the appearance of muscle tremors in a cool room can distort the electrocardiogram. The examination, as a rule, is carried out in a horizontal position, although nowadays examinations have also begun to be carried out in a vertical position, since in this case a change in autonomic support leads to a change in some electrocardiographic parameters [7].

It is necessary to record at least 6-10 cardiac cycles, and in the presence of arrhythmia, much more - on a long tape.

Normal electrocardiogram

On a normal ECG, 6 waves are distinguished, designated by the letters of the Latin alphabet: P, Q, R, S, T, U. The electrocardiogram curve (Fig. 1) reflects the following processes: atrial systole (P wave), artioventricular conduction (PR interval or, as it was previously designated as the P-Q interval), ventricular systole (QRST complex) and diastole - the interval from the end of the T wave to the beginning of the P wave. All waves and intervals are characterized morphologically: the teeth - by height (amplitude), and the intervals - by time duration, expressed in milliseconds. All intervals are frequency-dependent quantities. The relationship between heart rate and the duration of one or another interval is given in the corresponding tables. All elements of a standard electrocardiogram have a clinical interpretation.

Electrocardiogram analysis

The analysis of any ECG should begin with checking the correctness of its recording technique: to exclude the presence of various interferences that distort the ECG curve (muscle tremors, poor contact of electrodes with the skin), it is necessary to check the amplitude of the control millivolt (it should correspond to 10 mm). The distance between the vertical lines is 1 mm, which corresponds to 0.02 s when the belt moves at a speed of 50 mm/s, and 0.04 s at a speed of 25 mm/s. In pediatric practice, a speed of 50 mm/s is preferable, since against the background of physiological age-related tachycardia, errors are possible when calculating intervals at a tape speed of 25 mm/s.

In addition, it is advisable to take an ECG with a change in the patient’s position: in the wedge- and orthoposition, since in this case a change in the nature of autonomic support can contribute to a change in some parameters of the electrocardiogram - a change in the characteristics of the pacemaker, a change in the nature of the rhythm disturbance, a change in heart rate, a change in characteristics conductivity [2].

The general scheme of ECG analysis includes several components.

• Analysis of heart rate and conductivity: - determination of the source of excitation; - counting the number of heartbeats; — assessment of the regularity of heart contractions; — assessment of the conductivity function.
• Determination of rotations of the heart around the anteroposterior, longitudinal transverse axes: - the position of the electrical axis of the heart in the frontal plane (rotations around the anteroposterior, sagittal axis); — rotations of the heart around the longitudinal axis; - rotation of the heart around the transverse axis.
• Analysis of the atrial P wave.
• Analysis of the ventricular QRST complex: - analysis of the QRS complex; — analysis of the RS-T segment; - T wave analysis; - QT interval analysis.
• Electrocardiographic report.

Heart rate and conduction analysis

The source of excitation is determined by determining the polarity of the P wave and its position relative to the QRS complex. Sinus rhythm is characterized by the presence in standard lead II of positive P waves preceding each QRS complex. In the absence of these signs, a non-sinus rhythm is diagnosed: atrial, rhythm from the AV junction, ventricular rhythms (idioventricular), atrial fibrillation.

Counting the number of heartbeats is carried out using various methods. The most modern and simplest method is counting using a special ruler. If this is not available, you can use the following formula:

Heart rate = 60 RR,

where 60 is the number of seconds in a minute, RR is the duration of the interval, expressed in seconds.

If the rhythm is incorrect, you can limit yourself to determining the minimum and maximum heart rate, indicating this spread in the “Conclusion”.

Heart rate regularity is assessed by comparing the duration of RR intervals between successively recorded cardiac cycles. The RR interval is usually measured between the tips of the R (or S) waves. The spread of the obtained values ​​should not exceed 10% of the average duration of the RR interval. It has been shown that sinus arrhythmia of varying severity is observed in 94% of children. Conventionally, V degrees of sinus arrhythmia severity are distinguished:

I degree - there is no sinus arrhythmia or fluctuations in heart rate per 1 minute do not exceed 5 contractions;

II degree - mild sinus arrhythmia, rhythm fluctuations within 6-10 contractions per minute;

III degree - moderately severe sinus arrhythmia, rhythm fluctuations within 11-20 contractions per 1 minute;

IV degree - pronounced sinus arrhythmia, rhythm fluctuations within 21-29 contractions per 1 minute;

V degree - pronounced sinus arrhythmia, rhythm fluctuations within 30 or more contractions per minute. Sinus arrhythmia is a phenomenon inherent in healthy children of all ages [7].

In addition to physiologically observed sinus arrhythmia, abnormal (irregular) heart rhythm can be observed with various types of arrhythmias: extrasystole, atrial fibrillation and others.

Assessment of conduction function requires measurement of the duration of the P wave, which characterizes the speed of conduction of the electrical impulse through the atria, the duration of the PQ (PR) interval (conduction speed through the atria, AV node and His system) and the total duration of the ventricular QRS complex (conduction of excitation through the ventricles). An increase in the duration of intervals and waves indicates a slowdown in conduction in the corresponding part of the conduction system of the heart.

The PQ interval (PR) corresponds to the time it takes for an impulse to travel from the sinus node to the ventricles and varies depending on age, gender and heart rate. It is measured from the beginning of the P wave to the beginning of the Q wave, and in the absence of a Q wave, to the beginning of the R wave. Normal fluctuations in the PR interval are between 0.11-0.18 s. In newborns, the PR interval is 0.08 s, in infants - 0.08-0.16 s, in older ones - 0.10-0.18 s. Slowing of atrioventricular conduction may be due to vagal influence [1, 2].

The PR interval may be shortened (less than 0.10 s) as a result of accelerated impulse conduction, innervation disorders, due to the presence of an additional fast conduction path between the atria and ventricles. Figure 3 shows one of the options for shortening the PR interval.

This electrocardiogram (see Fig. 2) reveals signs of the Wolff-Parkinson-White phenomenon, including: shortening of the PR interval to less than 0.10 s, the appearance of a delta wave on the ascending limb of the QRS complex, deviation of the electrical axis of the heart to the left. In addition, secondary ST-T changes may be observed. The clinical significance of the presented phenomenon lies in the possibility of the formation of supraventricular paroxysmal tachycardia by the re-entry mechanism (re-entry of the impulse), since additional conduction pathways have a shortened refractory period and are restored to conduct the impulse faster than the main pathway [8].

Determination of the position of the electrical axis of the heart

Rotations of the heart around the anteroposterior axis. It is customary to distinguish three conventional axes of the heart, as an organ located in three-dimensional space (in the chest).

The sagittal axis is anteroposterior, perpendicular to the frontal plane, passing from front to back through the center of mass of the heart. Turning counterclockwise along this axis brings the heart to a horizontal position (displacement of the electrical axis of the QRS complex to the left). Rotate clockwise to a vertical position (displacement of the QRS electrical axis to the right).

The longitudinal axis anatomically runs from the apex of the heart to the right venous opening. When rotated clockwise along this axis (viewed from the apex of the heart), most of the anterior surface of the heart is occupied by the right ventricle; when rotated counterclockwise, the left ventricle is occupied.

The transverse axis passes through the middle of the base of the ventricles perpendicular to the longitudinal axis. When rotating around this axis, a displacement of the heart is observed with the apex forward or the apex backward.

The main direction of the electromotive force of the heart is the electrical axis of the heart (EOS). Rotations of the heart around the conventional anteroposterior (sagittal) axis are accompanied by deviation of the EOS and a significant change in the configuration of the QRS complex in standard and enhanced unipolar limb leads.

Rotations of the heart around the transverse or longitudinal axes are referred to as so-called positional changes.

The determination of EOS is carried out using tables. To do this, compare the algebraic sum of the R and S waves in standard leads I and III.

There are the following options for the position of the electrical axis of the heart:

• normal position when the alpha angle is from +30° to +69°;
• vertical position - alpha angle from +70° to +90°;
• horizontal position - alpha angle from 0° to +29°;
• axis deviation to the right - alpha angle from +91° to +180°;
• axis deviation to the left - alpha angle from 0° to - 90°.

The nature of the location of the heart in the chest, and, accordingly, the main direction of its electrical axis, is largely determined by the characteristics of the physique. In children with asthenic physique, the heart is located vertically. In children with a hypersthenic constitution, as well as with a high position of the diaphragm (flatulence, ascites), it is horizontal, with a deviation of the apex to the left. More significant turns of the EOS around the anteroposterior axis, both to the right (more than +90°) and to the left (less than 0°), are usually caused by pathological changes in the heart muscle. A classic example of deviation of the electrical axis to the right is the situation with a ventricular septal defect or tetralogy of Fallot. An example of hemodynamic changes leading to deviation of the electrical axis of the heart to the left is aortic valve insufficiency.

An easier way to roughly determine the direction of the EOS is to find the limb lead in which the R wave is the highest (without an S wave or with a minimal S wave). If the maximum R wave in lead I is a horizontal position of the EOS, if in lead II it is normal, if in lead aVF it is vertical. Registration of the maximum R wave in lead aVL indicates a deviation of the EOS to the left, in lead III - a deviation of the EOS to the right, but if the maximum R wave is in lead aVR, the position of the EOS cannot be determined.

Atrial P wave analysis

P wave analysis includes: change in P wave amplitude; measurement of P wave duration; determination of P wave polarity; determination of the shape of the P wave.

The amplitude of the P wave is measured from the isoline to the top of the wave, and its duration is measured from the beginning to the end of the wave. Normally, the amplitude of the P wave does not exceed 2.5 mm, and its duration is 0.10 s.

Since the sinus node is located in the upper part of the right atrium between the mouths of the superior and inferior vena cava, the ascending part of the sinus node reflects the state of excitation of the right atrium, and the descending part reflects the state of excitation of the left atrium, and it is shown that the excitation of the right atrium occurs before the left by 0. 02-0.03 s. The normal P wave is rounded in shape, gently sloping, with symmetrical rise and fall (see Fig. 1). The cessation of atrial excitation (atrial repolarization) is not reflected on the electrocardiogram, as it merges with the QRS complex. In sinus rhythm, the direction of the P wave is positive.

In normosthenics, the P wave is positive in all leads except lead aVR, where all electrocardiogram waves are negative. The largest value of the P wave is in standard lead II. In individuals of asthenic physique, the size of the P wave increases in standard III and aVF leads, while in lead aVL the P wave may even become negative.

With a more horizontal position of the heart in the chest, for example in hypersthenics, the P wave increases in leads I and aVL and decreases in leads III and aVF, and in standard lead III the P wave may become negative.

Thus, in a healthy person, the P wave in leads I, II, aVF is always positive, in leads III, aVL it can be positive, biphasic or (rarely) negative, and in lead aVR it is always negative.

Ventricular QRST analysis

The QRST complex corresponds to the electrical systole of the ventricles and is calculated from the beginning of the Q wave to the end of the T wave.

Components of the electrical systole of the ventricles: the QRS complex itself, the ST segment, the T wave.

The width of the initial ventricular QRS complex characterizes the duration of excitation transmission through the ventricular myocardium. In children, the duration of the QRS complex ranges from 0.04 to 0.09 s, in infants - no wider than 0.07 s.

The Q wave is the negative wave before the first positive wave in the QRS complex. The Q wave can be positive only in one situation: congenital dextracardia, when it is facing upward in standard lead I. The Q wave is caused by the spread of excitation from the AV junction to the interventricular septum and papillary muscles. This most variable ECG wave may be absent in all standard leads. The Q wave must meet the following requirements: in leads I, aVL, V5, V6, not exceed 4 mm in depth, or 1/4 of its R, and also not exceed 0.03 s in duration. If the Q wave does not meet these requirements, it is necessary to exclude conditions caused by a deficiency of coronary blood flow [2]. In particular, in children, anomalous origin of the left coronary artery from the pulmonary artery (ALCA from PA or Bluntd-White-Garland syndrome) often appears as a congenital pathology of the coronary vessels [2,3]. With this pathology, the “coronary” Q wave is most often persistently detected in lead aVL (Fig. 3).

The presented electrocardiogram (see Fig. 3) reveals a deviation of the electrical axis of the heart to the left. In lead aVL, the Q wave is 9 mm, with a height of R = 15 mm, the duration of the Q wave is 0.04 s. At the same time, in standard lead I, the duration of the Q wave is also 0.04 s, in the same lead there are pronounced changes in the final part of the ventricular complex in the form of depression of the ST interval. The suspected diagnosis of anomalous origin of the left coronary artery from the pulmonary artery was confirmed by echocardiography and then by coronary angiography.

At the same time, in infants, a deep Q wave may be in lead III, aVF, and in lead aVR the entire ventricular complex may have a QS appearance.

The R wave consists of ascending and descending knees, is always directed upward (except in cases of congenital dextracardia), reflects the biopotentials of the free walls of the left and right ventricles and the apex of the heart. The ratio of the R and S waves and the change in the R wave in the chest leads are of great diagnostic importance. In healthy children, in some cases, different sizes of the R wave are observed in the same lead - electrical alternans.

The S wave, like the Q wave, is an unstable negative ECG wave. It reflects a somewhat late coverage of excitation of distant, basal areas of the myocardium, supraventricular crests, conus arteriosus, and subepicardial layers of the myocardium.

The T wave reflects the process of rapid repolarization of the ventricular myocardium, i.e., the process of restoration of the myocardium or cessation of excitation of the ventricular myocardium. The state of the T wave, along with the characteristics of the RS-T segment, is a marker of metabolic processes in the ventricular myocardium. In a healthy child, the T wave is positive in all leads except aVR and V1. In this case, in leads V5, V6, the T wave should be 1/3-1/4 of its R.

The RS-T segment—the segment from the end of the QRS (the end of the R or S wave) to the beginning of the T wave—corresponds to the period of full coverage of the ventricles by excitation. Normally, an upward or downward displacement of the RS-T segment is permissible in leads V1-V3 of no more than 2 mm [4]. In the leads most distant from the heart (in standard and unipolar leads from the limbs), the RS-T segment should be on the isoline, with a possible upward or downward displacement of no more than 0.5 mm. In the left chest leads, the RS-T segment is recorded on the isoline. The transition point of the QRS to the RS-T segment is designated as the RS-T junction point j (junction).

The T wave is followed by a horizontal T-P interval, corresponding to the period when the heart is at rest (diastole).

The U wave appears 0.01-0.04 s after the T wave, has the same polarity and ranges from 5 to 50% of the height of the T wave. To date, the clinical significance of the U wave has not been clearly defined.

QT interval. The duration of ventricular electrical systole has important clinical significance, since a pathological increase in ventricular electrical systole may be one of the markers of the appearance of life-threatening arrhythmias.

Electrocardiographic signs of hypertrophy and overload of the heart cavities

Cardiac hypertrophy is a compensatory adaptive reaction of the myocardium, expressed in an increase in the mass of the heart muscle [6]. Hypertrophy develops in response to increased stress in the presence of acquired or congenital heart defects or with increased pressure in the pulmonary or systemic circulation.

Electrocardiographic changes in this case are caused by: an increase in the electrical activity of the hypertrophied part of the heart; slowing down the conduction of an electrical impulse through it; ischemic, dystrophic and sclerotic changes in the altered heart muscle.

However, it should be noted that the term “hypertrophy” widely used in the literature does not always strictly reflect the morphological essence of the changes. Often, dilatation of the heart chambers has the same electrocardiographic signs as hypertrophy, with morphological verification of the changes.

When analyzing the ECG, the transition zone (Fig. 4) in the precordial leads should be taken into account.

The transition zone is determined by the lead in which the R and S waves, i.e., their amplitude on both sides of the isoelectric line, are equal (see Fig. 4). In healthy older children, the QRS transition zone is usually determined in leads V3, V4. When the ratio of vector forces changes, the transition zone moves towards their predominance. For example, with right ventricular hypertrophy, the transition zone moves to the position of the left precordial leads and vice versa.

Signs of atrial overload

Electrocardiographic signs of left atrium overload form an electrocardiographic complex of signs, called P-mitrale in the literature. Enlargement of the left atrium is a consequence of mitral regurgitation with congenital, acquired (due to rheumatic carditis or infective endocarditis), relative mitral regurgitation or mitral stenosis. Signs of left atrium overload are presented in Figure 5.

Enlargement of the left atrium (see Fig. 5) is characterized by:

• an increase in the total duration (width) of the P wave by more than 0.10 s;
• widened double-humped P wave in leads I, aVL, V5-V6;
• the presence of a pronounced negative phase of the P wave in lead V1 (more than 0.04 s in duration and more than 1 mm in depth).

Since the lengthening of the P wave can be caused not only by an enlargement of the left atrium, but also by intra-atrial block, the presence of a pronounced negative phase of the P wave in lead V1 is more important when assessing overload (hypertrophy) of the left atrium. At the same time, the severity of the negative phase of the P wave in lead V1 depends on the heart rate and on the general characteristics of the wave voltage.

Electrocardiographic signs of overload (hypertrophy) of the right atrium form a complex of signs called P-pulmonale, since it develops in pulmonary pathology, as well as in chronic pulmonary heart disease. However, these conditions are uncommon in children. Therefore, the main causes of enlargement of the right atrium are congenital heart defects, such as Ebstein's tricuspid valve anomaly, as well as primary changes in the pulmonary artery - primary pulmonary hypertension.

Signs of right atrium enlargement are presented in Figure 6.

Enlargement of the right atrium (see Fig. 6) is characterized by:
• a high-amplitude P wave with a pointed apex in leads II, III, aVF, this sign is required in lead V1 or V2;
• with a P wave duration not exceeding 0.10 s.

In Figure 6, in addition to signs of right atrium overload, there are also signs of right ventricular overload.

Signs of ventricular overload (hypertrophy)

Since the ECG normally reflects the activity of only the left ventricle, electrocardiographic signs of left ventricular overload emphasize (exaggerate) the norm. Where the R wave is normally high (in lead V4, the position of which coincides with the left border of the heart), it becomes even higher; where the S wave is normally deep (in lead V2), it becomes even deeper.

Many voltage criteria for overload (hypertrophy) of the left ventricle have been proposed - more than 30. The most well-known include the Sokolov-Lyon index: the sum of the amplitudes of the R wave in lead V5 or V6 (where there is more) and S in lead V1 or V2 (where there is more ) more than 35 mm. However, the amplitude of the waves in the precordial leads is influenced by the gender, age and constitution of the patient. Thus, an increase in the voltage of the teeth can be observed in thin young people. Therefore, secondary changes in the final part of the ventricular complex are of great importance: displacement of the ST interval and T wave. As a sign of a relative deficiency of coronary blood flow, deepening of the Q wave in leads V5, V6 is possible. But at the same time, the Q wave should not exceed more than 1/4 of its R and 4 mm in depth, since this sign indicates a primary coronary pathology [2].

Predominant dilatation of the left ventricle has the following characteristics: R in V6 is greater than R in V5, greater than R in V4 and greater than 25 mm; sudden transition from deep S waves to high R waves in the precordial leads; shift of the transition zone to the left (towards V4) (Fig. 7).

Signs of predominant hypertrophy of the left ventricular myocardium are depression (displacement below the isoline) of the ST segment in lead V6, possibly also in V5 (Fig. [4, 7].

Electrocardiographic signs of overload (hypertrophy) of the right ventricle appear when its mass increases by 2-3 times. The most reliable sign of right ventricular hypertrophy is the qR complex in lead V1.

Additional signs are secondary changes in the form of ST segment displacement and changes in the T wave. In some pathological conditions, in particular with an atrial septal defect, right ventricular hypertrophy is also demonstrated by incomplete right bundle branch block in the form of rsR in lead V1 (Fig. 9) [ 7].

In conclusion, a standard electrocardiogram is very important for an adequate diagnosis, subject to several rules. This is, firstly, taking an electrocardiogram with a change in body position, which makes it possible to initially differentiate organic and inorganic damage to the heart. Secondly, this is the choice of the optimal shooting speed - for children 50 mm/s. Finally, the electrocardiogram should be analyzed taking into account the individual characteristics of the child, including his constitution.

For questions regarding literature, please contact the editor.

The editors apologize for typos

In the output of the article “Foot and Mouth Disease”, No. 8 2004, you should read:

A. E. Kudryavtsev, Candidate of Medical Sciences, Associate Professor, T. E. Lisukova, Candidate of Medical Sciences, Associate Professor, G. K. Alikeeva, Candidate of Medical Sciences Central Research Institute of Epidemiology, Ministry of Health of the Russian Federation, Moscow

In the article by I. Yu. Fofanova “Some issues of the pathogenesis of intrauterine infections”, No. 10.2004. On page 33 in the 2nd column from left to right it should be read: “In the second trimester (after clarification of the diagnosis), the use of antibacterial therapy is indicated, taking into account the sensitivity of antibiotics (penicillin or macrolides). Prescription of amoxiclav, augmentin, ranklav, azitrox, sumamed during pregnancy is possible only when the expected benefit to the mother outweighs the potential risk to the fetus or child. Despite the fact that experimental studies have not revealed the teratogenic effects of these drugs, their use during pregnancy should be avoided.”

E. V. Murashko, Candidate of Medical Sciences, Associate Professor of Russian State Medical University, Moscow

Treatment[edit]

It is important to understand that right ventricular hypertrophy itself is not the main problem, but what constitutes right ventricular hypertrophy is the issue. Right ventricular hypertrophy is an intermediate stage between increased right ventricular pressure (in early stages) and right ventricular failure (in later stages). [12] Therefore, treatment of right ventricular hypertrophy consists of either preventing the development of right ventricular hypertrophy or preventing progression towards right ventricular failure. Right ventricular hypertrophy itself has no (pharmacological) treatment. [6]

Treatment of the cause[edit]

Since the main causes of right ventricular hypertrophy are tricuspid regurgitation or pulmonary hypertension (discussed above), treatment includes treatment of these conditions. [3] Tricuspid regurgitation is usually treated conservatively, aiming to treat the underlying cause and regularly monitoring the patient. [13] Surgery is considered in more serious situations when the patient has severe symptoms. Surgical options include either valve replacement or valve repair (called annuloplasty). [3] When it comes to replacement, there is a choice between a bioprosthetic valve or a mechanical valve, depending on the specific characteristics of the patient. The mechanical valve has greater durability but requires anticoagulation to reduce the risk of thrombosis. [3] Treatment for pulmonary hypertension will depend on the specific cause of pulmonary hypertension. In addition, the following options may also be considered: diuretic, oxygen, and anticoagulant therapy. [3]

Complication management[edit]

After a long period, the right ventricle cannot adapt sufficiently to pump the increased pressure in the right ventricle, which is called right ventricular failure. This right ventricular failure is the main complication of right ventricular hypertrophy. The mechanisms underlying progression from hypertrophy to failure are not well understood [12], and the best treatment approach involves reducing/minimizing risk factors for progression. Lifestyle changes can often help reduce the risk of this progression. [5]Lifestyle changes include: eating less salty foods, since salt intake causes more fluid retention in the body; To give up smoking; Avoid excessive drinking, as alcohol reduces the force of heart contractions. When right ventricular hypertrophy progresses to right ventricular failure, treatment is reduced to heart failure. In short, this involves using: [ citation needed

]

• Diuretics
• 3 ACEi
• Beta blockers
• Aldosterone
• Antongists
• Cardiac glycosides
• Vasodilators

Left ventricular hypertrophy on ECG

LVH can occur for a number of reasons, one of the provoking factors is high blood pressure, the left ventricle works at an accelerated rhythm. First, the walls of the chamber thicken, which subsequently leads to loss of elasticity and deterioration in functional activity. In children, heart failure is usually associated with congenital heart defects.

Let us highlight the main reasons why left ventricular hypertrophy appears on the ECG:

• narrowing of the aortic valve;
• arterial hypertension;
• pathological enlargement of the heart muscle;
• grueling long-term strength physical activity;
• excess body weight.

Consider the clinical signs of left ventricular hypertrophy on the ECG:

• pain in the chest area;
• dyspnea;
• tachycardia;
• dizziness, even fainting;
• increased fatigue.

The left ventricle is the most important link in the circulatory system. It is responsible for supplying blood to tissues and organs, which is why hypertrophic changes will certainly affect the functioning of the most important systems of the body.

To avoid the development of serious complications, the pathological process should be identified in the early stages. To do this, when the first symptoms appear, you need to contact a cardiologist.

LVH can lead to the following complications, namely:

• heart failure;
• IHD;
• arrhythmia;
• myocardial infarction;
• cardiac arrest and death.

If we talk about left atrial hypertrophy, it occurs due to the following reasons: obesity, cardiomyopathy of various origins, pulmonary diseases, aortic stenosis, hypertension, stressful situations, etc.

Links[edit]

1. "Pulmonary hypertension". nhs.uk.
   _ NHS. March 14, 2022. Retrieved March 23, 2022.
2. ↑
   Ibrahim, Bassem (December 12, 2016).
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3. ^ abcdefghi Bhattacharya, Priyanka; Sharma, Sandeep (15 February 2022). "Right ventricular hypertrophy". StatPearls
   . NCBI. Retrieved March 23, 2022.
4. Oudiz, Ronald (21 June 2018). "Idiopathic pulmonary arterial hypertension". Medscape
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5. ^ ab "Understanding Right Ventricular Hypertrophy". Health line
   . 2018-02-09. Retrieved March 23, 2022.
6. ^ ab Johnson, John (16 August 2022). “What is right ventricular hypertrophy?” . Medical news today
   . Retrieved March 23, 2022.
7. ^ abc Nakamura, Michinari; Sadoshima, Junichi (April 19, 2018). "Mechanisms of physiological and pathological hypertrophy of the heart." Nature Reviews Cardiology
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8. Braz, Julian; Gregory, Kimberly (February 15, 2004). "PKC-α regulates cardiac contractility and susceptibility to heart failure." Natural Medicine
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9. Jump up
   ↑ Lehtonen, Jari (1988).
   "Electrocardiographic criteria for the diagnosis of right ventricular hypertrophy, confirmed at autopsy." Box
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10. Hancock, William (2009). "AHA/ACCF/HRS Guidelines for Electrocardiogram Standardization and Interpretation." Journal of the American College of Cardiology
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    (11):992–1002. DOI: 10.1016/j.jacc.2008.12.015. PMID 19281932.
11. Ho, Sue Yen (2006). "Anatomy, echocardiography and normal dimensions of the right ventricle". Heart
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12. ^ a b van der Bruggen, C (2017). "RV pressure overload: from hypertrophy to failure". Cardiovascular Research
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13. "Tricuspid regurgitation". BMJ Best Practice
    . BMJ. March 2022. Retrieved March 23, 2022.